Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The function and mechanism of aldh9a1b in diabetes

ABSTRACT: The function and mechanism of aldh9a1b in diabetes

PROVIDER: PRJNA925841 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23149200.fastq.gz	Fastqsanger.gz
	SRR23149188.fastq.gz	Fastqsanger.gz
	SRR23149189.fastq.gz	Fastqsanger.gz
	SRR23149190.fastq.gz	Fastqsanger.gz
	SRR23149191.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 13

Similar Datasets

The function and mechanism of aldh9a1b in diabetes

Project description:Reactive aldehydes such as 4-HNE, MDA and acrolein are implicated in the pathological development of diabetes as their widespread and universally exposed characteristics. Trans, trans-2,4-decadienal (tt-DDE) come from lipid peroxidation of omega-6 and is most abundant aldehyde in cooking oil fumes, while, its role in diabetes remained unknown. Aldh9a1 is a cytosolic enzyme that catalyze the NAD+-dependent oxidation of a variety of aldehydes and has its homology aldh9a1b in zebrafish. To investigate the function of endogenous and exogenous tt-DDE, aldh9a1b knockout zebrafish are established using CRISPR/Cas9 technology. TT-DDE was confirmed to act as substrate for aldh9a1b and a series of experiments are performed on a histological, metabolomic and transcriptomic level in aldh9a1b-/- zebrafish. Both aldh9a1b-/- larvae and adult fish displayed abnormal retinal vasculature and impaired glucose homeostasis, which are caused by tt-DDE induced downregulated insulin signaling pathway. Furthermore, the abnormal hyaloid vasculature in the fish can be reversed by insulin receptor sensitizer and metformin exhibited strongest effects among them. Altogether, these results identified tt-DDE as the preferred substrate for aldh9a1b, which subsequently causes microvascular damage and impaired glucose metabolism by insulin resistance.

2023-12-08 | GSE223340 | GEO

RFX6 haploinsufficiency predisposes to diabetes through impaired beta cell function

Project description:RFX6 haploinsufficiency predisposes to diabetes through impaired beta cell function

| PRJNA980693 | ENA

Targeted pharmacological therapy restores β-cell function for diabetes remission

Project description:Targeted pharmacological therapy restores β-cell function for diabetes remission

| PRJNA528110 | ENA

Serum exosomal miRNA profile in pregnancies with gestational diabetes based on pancreatic β-cell function

Project description:Pancreatic β-cell function impairment is a key mechanism for developing gestational diabetes mellitus (GDM). Maternal and placental exosomes regulate maternal and placental responses during hyperglycemia. Studies have associated exosomal micro RNAs (miRNAs) with GDM development. To date, no studies have been reported that evaluate the profile of miRNAs present in maternal and placental exosomes in the early stages of gestation from pregnancies that develop GDM. We used microarrays to assess whether early pregnancy maternal and placental exosomal miRNA profiles vary according to pancreatic β-cell function in women who will develop GDM (preGDM).

2024-02-29 | GSE243374 | GEO

Neonatal diabetes mutations disrupt a chromatin pioneering function that activates the human insulin gene

Project description:Despite the central role of chromosomal context in gene transcription, human noncoding DNA variants are generally studied outside of their endogenous genomic location. This limits our understanding of disease-causing regulatory variants. INS promoter mutations cause recessive neonatal diabetes. We studied 60 patients with such mutations, and show that all single base mutations disrupt a CC dinucleotide, while none affect elements important for INS promoter function in episomal assays. To model CC mutations, we humanized a ~3.1 kb region of the orthologous mouse Ins2 gene. This drove cell-specific transcription and recapitulated developmental chromatin states. A CC mutant allele, however, abrogated active chromatin formation during pancreas development. A search for transcription factors that act through this element revealed that another neonatal diabetes gene product, GLIS3, had a unique pioneer-like ability to derepress INS chromatin, which was hampered by the CC mutation. Our in vivo analysis, therefore, connects two human genetic defects in a pioneering mechanism that underlies developmental activation of the INS gene. This record contains the GLIS3 ChIP-seq and input control in human pancreatic islet cells revealing GLIS3 targets in human islet tissue.

2021-04-03 | GSE151405 | GEO

Discovering human diabetes-risk gene function with genetics and physiological assays

Project description:Discovering human diabetes-risk gene function with genetics and physiological assays

| PRJNA478311 | ENA

Function and Mechanism of METTL5-mediated translation in multiple myeloma

Project description:Function and Mechanism of METTL5-mediated translation in multiple myeloma

| PRJNA1250600 | ENA

Discovering human diabetes-risk gene function with genetics and physiological assays

Project description:To delineate the effects of BCL11A (a type 2 diabetes risk gene) in human beta cell function we knockdown BCL11A in primary human beta cells and generated and sequenced RNA-seq libraries from 4 human donors

2018-07-01 | GSE116369 | GEO

Transcriptome analysis reveals the molecular mechanism of Baduanjin in improving type 2 diabetes

Project description:Transcriptome analysis reveals the molecular mechanism of Baduanjin in improving type 2 diabetes

| PRJNA1152353 | ENA

PAX4 loss of function alters human endocrine cell development and influences diabetes risk [dataset 2]

Project description:Diabetes is a major chronic disease with an excessive healthcare burden on society. A coding variant (p.Arg192His) in the transcription factor PAX4 is uniquely and reproducibly associated with altered risk for type 2 diabetes (T2D) in East Asian populations, whilst rare PAX4 alleles have been proposed to cause monogenic diabetes8. In mice, Pax4 is essential for beta cell formation but neither the role of diabetes-associated variants in PAX4 nor PAX4 itself on human beta cell development and/or function are known. Here, we demonstrate that non-diabetic carriers of either the PAX4 p.Arg192His or a newly identified p.Tyr186X allele exhibit decreased pancreatic beta cell function. In the human beta cell model, EndoC-βH1, PAX4 knockdown led to impaired insulin secretion, reduced total insulin content and altered hormone gene expression. Deletion of PAX4 in isogenic human induced pluripotent stem cell (hiPSC)-derived beta-like cells resulted in de-repression of alpha cell gene expression whilst in vitro differentiation of hiPSCs from carriers of PAX4 p.192His and p.186X alleles exhibited increased polyhormonal endocrine cell formation and reduced insulin content. In silico and in vitro studies showed that these PAX4 alleles cause either reduced PAX4 expression or function. Correction of the diabetes-associated PAX4 alleles reversed these phenotypic changes. Together, we demonstrate the role of PAX4 in human endocrine cell development, beta cell function and its contribution to type 2 diabetes risk.

2023-08-05 | GSE203264 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data